Introduction

Substance use disorders involve excessive use of nicotine, alcohol, and other illicit substances
that leads to social, academic, and occupational impairment. The most common illicit
substances seen include cannabis, sedatives, hypnotics, anxiolytics, inhalants, opioids,
hallucinogens, and stimulants. The specific factors of substance use disorder consist of abuse,
intoxication, and physical/psychological dependence.
When a person uses a substance it can have various effects such as :
Acute intoxication: A transient condition following the use of alcohol or other psychoactive
substances resulting in alteration in level of consciousness, perception, mental functions,
behaviour and other physiological functioning. The level of alteration depends on the
quantity of substance used and blood levels of the substance.
Harmful use: A pattern of psychoactive substance use that is causing damage to health. The
damage can be in the form of physical damage (eg: alcohol liver disease) or psychological
(eg: episodes of depression secondary to alcohol consumption)
Addiction/ Dependence syndrome: A definitive diagnosis of dependence can be made only if
the following symptoms were present together at some point in the last year:
A regular pattern of substance use, especially early morning usage is present
Experience withdrawal symptoms when he/she does not use or reduce substance amount
F1x.0 Acute intoxication .00 Uncomplicated
.01 With trauma or other bodily injury .02 With other medical complications .03 With
delirium
.04 With perceptual distortions
.05 With coma
.06 With convulsions
.07 Pathological intoxication
F1x.1 Harmful use
F1x.2 Dependence syndrome
.20 Currently abstinent
.21 Currently abstinent, but in a protected environment
.22 Currently on a clinically supervised maintenance or replacement regime [controlled
dependence]
.23 Currently abstinent, but receiving treatment with aversive or blocking drugs
.24 Currently using the substance [active dependence]
.25 Continuous use
.26 Episodic use [dipsomania]
F1x.3 Withdrawal state .30 Uncomplicated
.31 With convulsions
F1x.4 Withdrawal state with delirium
1

.40 Without convulsions .41 With convulsions

F1x.5 Psychotic disorder
.50 Schizophrenia-like
.51 Predominantly delusional
.52 Predominantly hallucinatory
.53 Predominantly polymorphic
.54 Predominantly depressive symptoms .55 Predominantly manic symptoms
.56 Mixed
F1x.6 Amnesic syndrome
F1x.7 Residual and late-onset psychotic disorder .70 Flashbacks
.71 Personality or behaviour disorder .72 Residual affective behaviour
.73 Dementia
.74 Other persisting cognitive behaviour .75 Late-onset psychotic disorder
F1x.8 Other mental and behavioural disorders
F1x.9 Unspecified mental and behavioural disorder

Different substances can be classified based on their effects on the central nervous
system. These effects vary depending on the substance and can produce everything from
increased energy and euphoria to profound sedation. In general, while the effects vary
significantly, the initial stages of substance use disorders are characterized
by positive reinforcement, where individuals experience a sense of well-being or
euphoria with use. As physiological and psychological dependence progresses, an individual
experiences negative reinforcement where substances primarily relieve dysphoria and
unpleasant withdrawal symptoms.
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Etiology
The cause of substance use disorders is multifactorial and includes psychological, biological,
socio-cultural, and environmental factors. Co-morbid psychiatric disorders have been
associated with an increased risk of illicit substance use. For example, those with attention
deficit hyperactivity disorder (ADHD) and bipolar affective disorders have an increased risk
of developing a substance use disorder in adulthood compared to the general population.
Environmental and genetic factors also play a strong role in substance use
disorder. An individual's genetic make-up for stress-response predisposes the risk of
dependence on substances. Individual variations in genetics have been demonstrated to
influence stress response and predispose some individuals to develop a substance use
disorder.[1]
The Adverse Childhood Experience Study (ACES) demonstrated that exposure to a range of
traumatic events during childhood is associated with an increased risk of substance use later
in life. This risk association was demonstrated to follow a dose-response-like pattern where
increased trauma exposure was directly correlated with increased risk of developing a
substance use disorder.
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Epidemiology
The cause of substance use is multifactorial. It includes psychological, biological, socio-
cultural, and environmental factors. Some mental health disorders predispose individuals to
abuse illicit substances; for example, those with ADHD have a high chance of abusing illicit
substances in their adulthood.[1]
Cannabis is the most common abused drug in the United States.[2]
The Services Administration for Mental Health and Substance Abuse (SAHMSA), the
National Institute on Alcohol Abuse and Alcoholism (NIAAA), and the National Institute of
Drug Abuse (NIDA) have accumulated data on substance use and its consequences over the
years. Studies show individuals who abuse one substance are more like to abuse other
substances as well. In 2012, studies showed that the lifetime prevalence of alcohol use
disorder was 8%, and illicit substance use was 2-3%.[3]
A cross-sectional study was conducted in the US with 36,309 adults, and the data was
obtained from April 2012 to June 2013. The study showed a 12-month prevalence of
substance use disorder was 3.9% and lifetime substance use disorder was 9.9%. Substance
use disorder was more prominent among certain population groups. They were men,
Caucasian, Native Americans, young single or previously married adults, lower educated
individuals, lower-income individuals, and those residing on the Western side of the country.
There was a significant association with individuals with disabilities, with a 12-
month prevalence of 13.5% and a lifetime prevalence of 24.6%.[4]
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Pathophysiology
Substance use disorders involve both psychological and physical dependence on the
substance(s) of use. Severe dependence is characterized by an inability to regulate use.
Substance use disorders and addiction stem in part from adaptive changes in the brain as
it seeks to regain homeostasis.[5] Chronic and/or prolonged stress plays a strong role in
developing drug-seeking behavior; it alters the corticotropin-releasing factor and
hypothalamic-pituitary-adrenal axis (CRF/HPA)". In animal model studies, it demonstrated
CRF circuitry could increase "dopamine activity in the mesolimbic reward circuit."[6]
Stimulants, specifically cocaine and amphetamines, exert their effect by preventing the
recycling of dopamine, norepinephrine, and serotonin. This results
in increased concentrations of these neurotransmitters within the synaptic cleft. The influx of
these neurotransmitters gives the user a euphoric effect.[7]
Worldwide and in the United States, tobacco use disorder is the most prevalent
addiction. Most commonly, nicotine is absorbed through the lungs when individuals burn
and inhale tobacco products. It is absorbed through the pulmonary circulation, crosses the
blood-brain barrier in less than 10 seconds, and attaches to the nicotinic cholinergic
receptors in the central nervous system (CNS). The metabolite of nicotine is cotinine, which
can be detected as a urinary marker of the substance.[8] Nicotine influx in the CNS leads to
neurotransmitters' release, especially dopamine, which stimulates the brain’s
reward area. Chronic nicotine use results in tolerance, when excessive stimulation of nicotine
acetylcholine receptors results in desensitization of the receptors;
these neuroadaptations produce a state where the brain requires nicotine to function in
homeostasis. This is referred to as physiological dependence.[9] CYP2D6 metabolizes
nicotine. Therefore, it can alter the metabolism of other medications, such as antipsychotics.
Alcohol produces euphoric effects through the dopamine neurons of the mesolimbic system.
Alcohol inhibits NMDA receptors and results in the upregulation of GABA
receptors. Chronic consumption of alcohol leads to GABA receptor desensitization and
tolerance, potentiating the loss of drinking control.[10] Alcohol is mostly absorbed in the
digestive tract's mucosal lining, specifically at the proximal small intestine, where B vitamins
are absorbed. Individuals who drink excessively may have a deficiency of B
vitamins.[11] Vitamin B1 (Thiamine) and vitamin B9 (Folic Acid) are the two most common
B-vitamins deficiencies. Deficiency of thiamine can lead to neurological findings such as
hyporeflexia and sensory and motor deficiency. More profound deficiencies over time
can lead to Wernicke's Encephalopathy and Korsakoff syndrome [12]. Chronic alcohol
consumption can also result in Vitamin B9 (Folic acid) deficiency; after 8-16 weeks of
deficient stores of folic acid in the body, individuals may develop "glossitis, angular
stomatitis, and oral ulcers," along with "depression, irritability, insomnia, cognitive decline,
fatigue, and psychosis."[13]
Opioids include codeine, heroin, hydrocodone, hydromorphone, methadone, meperidine, mor
phine, and oxycodone. Opioids bind to delta, kappa, and mu receptors,
which provide analgesia for severe pain and produce euphoria feelings. Higher doses carry a
risk of respiratory suppression and death. Individuals with chronic exposure to opioids can
experience profound withdrawal symptoms if opioid use is stopped abruptly. The withdrawal
symptoms include but are not limited to diarrhea, excess sweating, excess lacrimation,
nausea, vomiting, and insomnia.[14]
Sedative, Hypnotic, Anxiolytics are a class of medications that can cause CNS depression,
and if taken inappropriately, the effects can be fatal. They
include benzodiazepines: alprazolam, clonazepam, lorazepam, diazepam, chlordiazepoxide;
Barbiturates: phenobarbital, pentobarbital, butabarbital; it also includes other sedative
medications. Other classes of drugs have properties that share a similar mechanism of
action with benzodiazepine and barbiturates. These agents mediate gamma-aminobutyric acid
(GABA) effects, producing inhibitory effects within the central nervous system. Alcohol can
be classified in this group, but alcohol is more commonly used and is not utilized
therapeutically, so healthcare experts have classified it separately.[15] The euphoric and
sedative effects of these agents precipitate and perpetuate a cycle
of overuse and dependence.
Regarding cannabis, it contains multiple types
of terpenophenolic compounds, called cannabinoids, that cross the blood-brain barrier; the
most studied cannabinoids are cannabidiol (CBD) and tetrahydrocannabinol
(THC). Cannabinoids act on the cannabinoid receptors, which are located in the central and
peripheral nervous system. CBD and THC both come from the hemp plant, also known as
marijuana; legal rules and regulations differentiate the definitions. There are many types of
hemp plants that produce various percentages of THC and CBD. Hemp has less than or equal
to 0.3% of THC by dry weight, while marijuana has more than 0.3 % of THC by dry
weight. CBD is a non-psychotropic cannabinoid that does not exert euphoric
properties like THC.[16] THC, the psychoactive cannabinoid, exerts its effects in the brain’s
reward center in increasing dopamine levels in the prefrontal cortex, providing the euphoric
effect.[2] THC activates the CB1 and CB2 receptors of the endocannabinoid system, which
gives its psychoactive properties and regulating eating, learning, memory, growth,
development, and anxiety.[17] CBD does not activate CB1 or CB2 receptors, but limited
studies show it has neuroprotective and anti-inflammatory effects.[18]
There are various hallucinogens; the most common one presented in the hospitals is
phencyclidine or phenylcyclohexyl piperidine (PCP), or also known by its street name
"angel dust," is not only a hallucinogen but also acts as a stimulant. Its mechanism of action
is characterized by NMDA receptor antagonism impairing the feeling of pain and other
various neurological functions and psychosis. It can also facilitate the increase of dopamine
and norepinephrine and provide a sympathomimetic effect.[19] Another common
hallucinogen is Lysergic acid diethylamide (LSD), or known by its street name as "acid";
it has a mechanism of action that is not fully understood, but from studies so far,
it facilitates serotonin receptors 5HT2A, 5HTAR, 5HT2C, and 5HT1A. LSD exerts receptor
modulation leading to cognitive impairment and hallucinations. Other hallucinogens include
MDMA with street names of “Molly, Ecstasy, X,” another hallucinogen is Ketamine with a
street name of “K-Hole.”
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History and Physical

In addition to the physical exam, assessment of substance use should include a thorough
history that screens several psychiatric symptoms to diagnose and rule out disorders. The
patient should be asked about any current life stressors, and the patient should be screened
for current depression, mania, trauma, anxiety, and psychosis.
Current substance use screening questions include:
• Which substance(s) are used? Certain substances can cause more negatives effects
than others, so it is important to determine which ones were used, which may help in
the recovery process.
• When was the last time the substance was used, and how much and how often was it
used? The negative consequences of withdrawal symptoms may be fatal, such as from
benzodiazepines or alcohol. If the provider was notified of the last use,
then appropriate treatment can be administered on time. Also, recent substance use
can influence an individual’s behavior and cognitive processes, such as being agitated
from Methamphetamine or Cocaine. This would help in the treatment process. For
example, a patient may not need inpatient admission if the exhibited psychotic
 symptoms were substance-induced instead of a psychotic episode of Schizophrenia.
The frequency of substance use helps determine the severity of the dependency.
• Any experience of withdrawal symptoms? Some substance use can lead to severe
withdrawal symptoms. Alcohol and Benzodiazepine withdrawal can lead to seizures
and have the potential to be fatal.
• What is the user’s perception of using the substance(s)? How an individual perceives
illicit substances will vary from person to person. Some individuals use substances to
cope with life stressors, while others may use it as an alternative to medications such
as cannabis for treating their anxiety.
• Any feelings or readiness to change, such as cutting back use or quitting? Does the
patient have any cravings for the substance?
Past Psychiatric History: if the patient has any psychiatric
history, detailed information regarding mental health history should be obtained. When
asking about a period in the past, it is easier to have the patient recall an event by age than
recall the year. The questions to ask include:
• Have you been diagnosed with any psychiatric diagnosis in the past by a
physician? This question should be asked, and it should be verified if the diagnosis
was made by a medical professional or if someone else told them the diagnosis.
• Any history of medication trials for substance use or other mental health
disorder? This open-ended question may not have a complete answer because the
patient may have difficulty recalling the complicated names of medications from the
past. If the patient affirms taking medications but cannot recall the name, an effective
way to get the information is to call the pharmacy to get the list or get the medical
records from their last prescriber.
• Any history of self-harm or attempted suicide? Perceptual disturbance during an
intoxicated state may lead to hallucinations, such as having bugs or snakes on their
skin. The visual hallucinations may lead to self-harm to rid self of the hallucinations.
Also, auditory hallucinations of commanding nature may result in a suicide attempt. If
past suicide attempts are identified, then it is recommended to ask when the first
attempt was, how many were attempted, and what lead to the suicide attempts,
• Any history of violence towards others? A study regarding ED visits due to Cocaine-
induced chest pain found 40% of the patients were involved in violence a year after
discharge from the ED.[20] Substance abuse can cause loss of impulse control and
agitation, in which the user will have mood dysregulation leading to violent behavior.
Obtaining history about the patient’s history of violence enables the provider to assess
for any future risks.
• At what age were the first and last psychiatric hospitalization? How many
hospitalizations regarding substance use or other mental health illness can you
recall? These questions should be asked in more detail and asked about the
differences of being treated in the ED, such as for psychiatric stability or due to
intoxication, and if the patient was admitted to inpatient for stabilization. Those who
are treated in the ED due to intoxication usually are stabilized and discharged after a
day. But those admitted to the inpatient for psychiatric care are admitted for at least 5
days or so until they are psychiatrically stabilized.
Substance Use History Questions:
• At what age did the individual initiate use of the substance? This question is
asked because substance use affects brain development and can influence
impulsive/risky behaviors from an early age. Substance use at an early age can
predispose people to be cardiac and neurological disorders in adulthood.
• What benefit is sought out from substance use? Those who use substances may not
always use them for recreational use. Some may use it for self-treatment of their co-
morbid psychiatric or medical illnesses or dealing with stress. For example, those
who are diagnosed with ADHD may use Cocaine or Methamphetamine as an aid
to focus. Some may use Cannabis to treat their anxiety, insomnia, or neuropathic
pain. Therefore, it is important to be aware of what is the motivation behind substance
use.
• Has the individual ever attempted to cut back or stop using? This question helps
to determine the motivation for change. It should be followed up by questions
assessing periods of success and potential barriers to implementing strategies to
reduce or eliminate use.
• Has the patient previously received treatment for a substance use
disorder? Treatment options can include community self-help groups, outpatient
treatment clinics, intensive outpatient programs, medical detoxification, or residential
treatment facilities (Rehab)
• Is there a family history of drug use? If so, have there been any fatalities from
substance use? It is important to be aware of any substance use by other family
members because family influences the individual’s risk of substance use.
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Evaluation
Evaluation of the patient initially involves approaching the patient in a non-
judgmental manner. The provider's diction should concentrate on recovery and goal
setting. How well the first interview is conducted sets the tone for establishing a good rapport
between the provider and patient. The provider should always complete the history and
physical for assessment. Additionally, the healthcare provider should obtain a full set of
labs to help the health provider assess the patient’s health. The lab tests that are
recommended include:
• Blood Alcohol Level and Urine Drug Screen to screen for acute substance use. It
is usually done in the Emergency Room if the
patient exhibits agitation, sedation, or cognitive impairment. Urine pregnancy tests
should also be obtained when appropriate.
• Complete Blood Count (CBC) may show anemia and infection, while Basic
Metabolic Panel (BMP) will show any abnormal electrolyte
imbalance regarding substance use and any other co-morbidity.
• Liver Function Test and Hepatitis Panel can help show any negative effects on the
liver from chronic alcohol use or other substances; it can also show any hepatitis
B & C infections from IV drug use. HIV antibody test should also be added to rule out
any infection from IV drug use.
 • Pancreatic Enzyme's serum level can show any issues with the pancreas from alcohol
binge drinking or heavy nicotine use.
For establishing a diagnosis based on substance use, the DSM-5 is used. Per DSM-5, the
individual must meet at least two criteria out of 11 criteria, over a 12-month period, to have
substance use disorder established for that substance. Overall, the criteria are similar among
the substances. PCP Use Disorder does not have a withdrawal criterion established, so there
are only 10 criteria for that disorder. Some stimulants, opioids, sedatives, anxiolytics, and
hypnotics can be used under a physician’s supervision, so tolerance is omitted for individuals
taking them for treatment purposes. The 11 problems include:
1. The substance use amount is taken more than what was intended and taken longer
than what was intended.
2. There is the intention and failed attempts to decrease use.
3. Extra time and effort are used to obtain and use the substance or recover after
taking them.
4. Having a strong craving for the substance.
5. The use of the substance leads to the individual unable to fulfill his or her
responsibility.
6. Continued use of the substance despite having social and occupational impairment
due to the substance use.
7. Other activities are reduced or given up due to continued substance use.
8. Using the substance in a high-risk setting, such as when operating a motor vehicle
or operating heavy machinery
9. Continued use of the substance with the knowledge of the psychological and physical
harmful effects caused by the substance.
10. Tolerance development either from taking more amount of the substance to reach the
same effect from last time or from having decreased effect from using the same
amount of the substance.
11. Withdrawal symptoms are manifested after the substance use is discontinued, and the
withdrawal symptoms are relieved with the continuation of substance use.
The number of criteria the patient meets determines the severity level of the disorder; 2-3 sets
the severity level as mild, 4-5 sets the severity level as moderate, and 6 or more sets the
severity level as severe. A patient can relapse after reaching remission. For the patient to be
in remission, the patient must meet at least 2 criteria, which are listed above, over a 12-
months period, and be abstinent from substance use for at least 3 months. The period
of time from 3-12 months where symptoms are in remission is referred to as
early full remission; after 12 months, the condition is classified as sustained remission.
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Treatment / Management
Currently, nicotine, alcohol, and opioids are the only substances with FDA-approved
medication treatments. Individuals with severe addiction may require assistance in a
structured environment for the recovery process. The American Society of Addiction
Medicine (ASAM) provides a set of criteria for individualized treatment planning and
placement of individuals with addiction. The ASAM criteria involve
six dimensions: intoxication/withdrawal potential, medical condition and history, mental
health, individual's willingness to change, relapse/continue use potential, and recovery/living
situation.[21] Patients who require further assistance after being discharged from 24-hour
inpatient care or do not qualify for inpatient care may receive treatment
from intensive outpatient programs (IOPs). IOPs do not require patients to be admitted.
Instead, the patients can stay in their homes while they are treated in an outpatient clinic for
substance use during the day. IOPs comprise psychosocial support, developing coping skills,
and any other needed services individually.[22]
To treat nicotine use disorder, bupropion, varenicline, and nicotine replacement therapy are
available.
Bupropion is a dual reuptake inhibitor of dopamine and norepinephrine, which helps with
nicotine cravings and withdrawal symptoms.[23] Varenicline has a strong affinity to nicotinic
acetylcholine receptors and acts as a partial agonist, reducing withdrawal symptoms and
blocking nicotine binding. It provides the same stimulation as nicotine and decreases the urge
to use nicotine. Also, varenicline does not interact with CYP450 enzymes, which can
be beneficial when treating patients with other medications metabolized through the CYP450
pathway.[24] Nicotine replacement therapy (NRT) with patches and nicotine gum help with
cravings and withdrawal symptoms. Some studies show a combination of the gum and the
patch improves smoking cessation rates.[25] In any clinical setting, healthcare
providers should provide education and resources for smoking cessation, as the health
benefits of smoking cessation are significant.
For stimulant use disorder, such as with cocaine and amphetamine drugs, there are no
approved pharmacological treatments.[26] However, non-pharmacological therapy, such
as contingency management, is available; it involves operant conditioning reinforcement. The
goal of the treatment is to influence a certain type of behavior via behavioral rewards. In
substance use, behavior is modified by providing a reward in exchange for the desired
behavior, such as decrease substance use or abstinence.[27]
The FDA approves acamprosate, naltrexone, and disulfiram to treat alcohol use
disorder.[28] Disulfiram, an aldehyde dehydrogenase inhibitor, produces an unpleasant set of
symptoms such as headache, nausea, vomiting, flushing, dizziness, and weakness when
alcohol is consumed to prevent further alcohol consumption.[29] Naltrexone blocks the
central mu-receptor, reducing cravings, and aids in preventing relapse to alcohol
use.[30] Acamprosate aids in reducing withdrawal symptoms by countering excessive
NMDA receptor activation from alcohol withdrawal. In the clinical setting, it is important
to include vitamin B1 and vitamin B9, along with multivitamins supplements, to address any
nutritional deficiencies.
For opioid use disorder, several treatment options are available. They include methadone,
naltrexone, and buprenorphine, which are frequently combined with naloxone to reduce the
risk of misuse. Methadone (full mu agonist) can only be used to treat opioid use disorder by
specific treatment facilities designated as Opioid Treatment Programs (OTPs). Methadone
has decades of research demonstrated reduced illegal drug use, criminal activity, mortality,
and morbidity, buprenorphine-naloxone (partial agonist at the mu-opioid receptor). As a
partial agonist, this agent has less potential for overdose.[14] During opioid withdrawal, the
patient can experience dysregulated mood, dyssomnia, pupillary dilation, muscle pain,
nausea, vomiting, excessive lacrimation, and other symptoms. The (Clinical Opiate
Withdrawal Scale) COWS scale is an 11-item rating system used to measure the severity of
opioid withdrawal; a score of 5 or above indicates active withdrawal. Clonidine, an alpha-2
receptor agonist, may help reduce the severity of withdrawal symptoms and stabilize blood
pressure. Loperamide may also be needed to aid the patient's GI effect in the setting of
repeated diarrhea during withdrawal.[31]
Mainstreaming Addiction Treatment (MAT) Act
The Mainstreaming Addiction Treatment (MAT) Act provision updates federal guidelines to
expand the availability of evidence-based treatment to address the opioid epidemic. The
MAT Act empowers all health care providers with a standard controlled substance license to
p escribe buprenorphine for opioid use disorder (OUD), just as they prescribe other essential
medications. The MAT Act is intended to help destigmatize a standard of care for OUD and
will integrate substance use disorder treatment across healthcare settings.
As of December 2022, the MAT Act has eliminated the DATA-Waiver (X-Waiver) program.
All DEA-registered practitioners with Schedule III authority may now prescribe
buprenorphine for OUD in their practice if permitted by applicable state law, and SAMHSA
encourages them to do so. Prescribers who were registered as DATA-Waiver prescribers will
receive a new DEA registration certificate reflecting this change; no action is needed on the
part of registrants.
There are no longer any limits on the number of patients with OUD that a practitioner may
treat with buprenorphine. Separate tracking of patients treated with buprenorphine or
prescriptions written is no longer required.
Pharmacy staff can now fill buprenorphine prescriptions using the prescribing authority's
DEA number and does not need a DATA 2000 waiver from the prescriber. However,
depending on the pharmacy, the dispensing software may still require the X-Waiver
information in order to proceed. Practitioners are still required to comply with any applicable
state limits regarding the treatment of patients with OUD. Contact information for State
Opioid Treatment Authorities can be found
here: https://www.samhsa.gov/medicationassisted-treatment/sota.
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Differential Diagnosis
• Depression can be exhibited from opioids, alcohol, sedative, anxiolytic, hypnotic, and
cannabis use. It is also associated with withdrawal from stimulants.
• Mania and anxiety can be exhibited from stimulants (cocaine and amphetamine).
• Psychosis can be associated with substances but varies from individual to individual
and with time.
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Toxicity and Adverse Effect Management

Patients who are physically dependent on sedative effects often require medication during
the detoxification process to minimize the risks associated with complicated withdrawal.
Acute intoxication can present with slurred speech, cognitive impairment, poor coordination,
and unsteady gait. For alcohol and benzodiazepine withdrawal, the Clinical Institute
Withdrawal Assessment (CIWA) scale helps determine the frequency of medication dosing to
prevent withdrawal complications. In an emergency setting, treatment for alcohol and
benzodiazepine intoxication is primarily supportive, with close monitoring
of vitals. Benzodiazepines are considered a first-line treatment to prevent worsening
withdrawal symptoms.[32] In cases of severe benzodiazepine intoxication, particularly if the
patient is becoming hypoxic, flumazenil may be indicated. Flumazenil reduces the expression
of GABA subunit receptors, reversing the effect of benzodiazepines.[33]
For opioid intoxication, naloxone is used to reverse respiratory depression caused by opioid
overdose. Naloxone is a competitive mu-opioid receptor antagonist, which reverses the
effects of opioids. It can be administered intramuscularly, intravenously, or nasally; the
fastest route of administration is intravenous.[34]
For PCP intoxication, the focus is stabilizing the patient with supportive care. The
patient may exhibit ataxia, nystagmus, increase cardiac workload, muscle rigidity, and
seizures. Hyperacusis is another side-effect of PCP use, which is why it may be necessary to
place the patient in a low stimulus environment. A high stimulus environment may
trigger agitation and increase the likelihood that restraints are required. In some cases,
gastric suction or the use of activated charcoal may be indicated. Benzodiazepines may help
to control agitation and reduce the risk of seizures.[19]
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Staging
During the recovery process of substance use, the individual transitions through various
stages of change, demonstrated as the stages of change model.
1. Precontemplation, when the individual does not recognize the negative effects of
substance use.
2. Contemplation, when the issues of substance use are recognized, yet no action is
taken.
3. Preparation, when the individual has considered making a
change regarding substance use and begins to make minor changes.
4. Action is the stage when the individual makes significant changes to prevent
substance use, such as avoiding triggers or reaching out for help.
5. Maintenance, the stage when the action stage is maintained to prevent substance use.
6. Relapse, the stage when the substance use is restarted.[35]
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Prognosis
Individuals who abuse substances for a chronic period develop extreme dependence on them.
If the individual attempts to stop using it, their withdrawal symptoms become severe enough
for the individual to restart the abuse cycle. There are predicting factors that influence the
outcome for the individual; the degree of relationship between the predictor factor and the
outcome varies from person to person. Some of the predicting factors include but not limited
to are the degree of dependence and withdrawal, the motivation to be committed to
abstinence, treatment timeframe, genetics, the severity of cravings, and how the individual
copes during stressful situations.[36]
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Complications
The complications of substance use are broad.
Substance use will impact multiple systems of the body, including but not limited to
neurologic, endocrine, psychiatric, cardiopulmonary, hepatic, hematologic,
and immunologic. These problems include but not limited to are:
• Stroke and seizures
• Loss of nerve functions leading to muscle weakness and loss of sensation.
• Memory loss and overall cognitive deficits.
• Various forms of psychosis, loss of impulse control, personality change, and mood
dysregulation.
• Coma and death
• Increased cardiac workload and with chronic use cardiac failure.
• Nasal Septal Perforation
• Respiratory depression
• Muscle breakdown from overuse, leading to rhabdomyolysis.
• Liver failure and hepatocellular carcinoma
• Hepatitis B & C infections, HIV, sepsis, and gangrene

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